Objective. This was a comparative study between FNAC and thyroid scan used to diagnose the solitary thyroid nodule and histopathology was used as gold standard to compare the results of both modalities. We hypothesized that Fine needle aspiration cytology and thyroid scan diagnose solitary thyroid nodule (STN) as accurately as histopathology. Materials and Methods. This study comprised of 50 patients with solitary thyroid nodules (STN) presented to OPD. After clinical examination these patients were referred to Centre for Nuclear Medicine, Mayo Hospital Lahore for thyroid function tests and thyroid scan (TS). These patients underwent FNAC in the department of Pathology and surgery in Mayo Hospital. The cases were operated and evaluated for histopathological changes. Results. On thyroid scan, 40 patients (80%) having cold nodule were labeled as suspicious 10 patients (20%) had hot nodule. On FNAC 23 patients (46%) had benign lesion, 22 patients (44%) had indeterminate lesion and 5 patients (10%) had malignant lesions. On histopathology, 45 patients (90%) were confirmed to have benign lesions and 5 patients (10%), malignant lesions. After comparison of results of thyroid scan and FNAC with histopathology, the sensitivity, specificity, positive predictive value, negative predictive value and diagnostic accuracy of thyroid scan were 80%, 20%, 10%, 90% and 26%, respectively whereas those of FNAC were 80%, 97.7%, 80%, 97.7% and 96%, respectively. Conclusion. Fine needle aspiration was a significantly better predictor of malignancy than thyroid scan and resulted in a smaller proportion of excisions for benign nodules.

This study explored the roles of activins and follistatin in colorectal cancers. Paired malignant and normal colonic tissues were collected from archived paraffin-embedded (n = 90 patients) alongside fresh (n = 40 patients) specimen cohorts. Activin β-subunits, follistatin and Smad4 mRNAs and proteins were measured by real-time PCR and immunohistochemistry (IHC). Mature activin-A, -B, -AB and follistatin proteins were measured by ELISA. Cancer tissues having ≤ the 20th percentile of the Smad4 IHC score were considered as low (L-S4) group. The Smad4-intact SW480 and Smad4-null HT29 colon cancer cell lines were treated with activins and follistatin, and cell cycle was analysed by flow cytometry. The cell cycle inducing (CCND1/CCND3) and inhibitory (p21/p27) proteins alongside the survival (survivin/BCL2) and pro-apoptosis (Casp-8/Casp-3) markers were measured by immunofluorescence. Thirty-nine patients had right-sided cancers (30%) and showed higher rates of L-S4 tumours (n = 17; 13.1%) alongside worse clinicopathological characteristics relative to left-sided cancers. The βA-subunit and activin-A increased, whilst βB-subunit and activin-AB decreased, in malignant sites and the late-stage cancers revealed the greatest abnormalities. Interestingly, follistatin declined markedly in early-stage malignant tissues, whilst increased significantly in the advanced stages. All activin molecules were comparable between the early stage right- and left-sided tumours, whereas the late-stage right-sided cancers and L-S4 tumours showed more profound deregulations. In vitro, activin-A increased the numbers of the SW480 cells in sub-G1 and G0/G1-phases, whereas reduced the HT29 cell numbers in the sub-G1 phase with simultaneous increases in the G0/G1 and S phases. The p21/p27/Casp-8/Casp-3 proteins escalated, whilst CCND1/CCND3/BCL2/survivin declined in the SW480 cells following activin-A, whereas activin-A only promoted p21 and p27 alongside reduced CCND3 in the HT29 cells. By contrast, activin-AB increased the numbers of SW480 and HT29 cells in Sub-G1 and G0/G1-phases and promoted the anti-cancer and reduced the oncogenic proteins in both cell lines. In conclusion, activins and follistatin displayed stage-dependent dysregulations and were markedly altered during the advanced stages of right-sided and L-S4 cancers. Moreover, the activin-A actions in CRC could be Smad4-dependent, whereas activin-AB may act as a Smad4-independent tumour suppressor protein.

Small cell carcinoma of the ovary, hypercalcemic type (SCCOHT) is a very rare and lethal tumor, mostly affecting young women, with aggressive clinical course. It has a worse prognosis in younger women and most of them died within two years of diagnosis. We are reporting a unique case of SCCOHT in a 35 years old, nulliparous lady with primary infertility in which symptomatic hypercalcemia was a presenting feature of her cancer. She was completely healthy before third cycle of IVF. Within two months of her third IVF cycle, she developed SCCOHT with a very rapid and aggressive course of disease and fatal outcome. Patient died within one month of her first symptom presentation (3 months after IVF cycle).

Leptomeningeal carcinomatosis (LMC) is a diffuse or multifocal malignant infiltration of the pia matter and arachnoid membrane. The most commonly reported cancers associated with LMC are breast, lung, and hematological malignancies. Patients with LMC commonly present with multifocal neurological symptoms. We report a case of LMC secondary to gastroesophageal junction cancer present initially with cauda equina syndrome. A 51-year-old male patient with treated adenocarcinoma of the gastroesophageal junction presented with left leg pain, mild weakness, and saddle area numbness. Initial radiological examinations were unremarkable. Subsequently, he had worsening of his leg weakness, fecal incontinence, and urine retention. Two days later, he developed rapidly progressive cranial neuropathies including facial diplegia, sensorineural hearing loss, dysarthria, and dysphagia. MRI with and without contrast showed diffuse enhancement of leptomeninges surrounding the brain, spinal cord, and cauda equina extending to the nerve roots. Cerebrospinal fluid cytology was positive for malignant cells. The patient died within 10 days from the second presentation. In cancer patients with cauda equina syndrome and absence of structural lesion on imaging, LMC should be considered. To our knowledge, this is the first case of LMC secondary to gastroesophageal cancer presenting with cauda equina syndrome.